Kalckar H M, Ullrey D
Proc Natl Acad Sci U S A. 1973 Sep;70(9):2502-4. doi: 10.1073/pnas.70.9.2502.
Enhancement of hexose uptake seems well correlated with transformation of cell cultures by tumor viruses and the absence of contact inhibition. Enhancement of sugar uptake has also been observed as a result of hexose starvation. Both types of enhancement can clearly be demonstrated in cultures of hamster cells when uptake of (14)C-labeled galactose is monitored after 10 or 20 min. The profiles of accumulation products are strikingly different. In cultures of hamster NIL cells transformed with polyoma virus much of the (14)C is accumulated as UDPhexose. Untransformed cells accumulate galactose-l-phosphate as well as UDPhexose. Hexose-starved cells show enhanced uptake of galactose; however, this marked enhancement was only observed in NIL cultures close to contact inhibition. The novel and common feature seen in hexose-starved cells when incubated briefly with (14)C-labeled galactose is the occurrence of a marked accumulation of [(14)C]UDPglucuronic acid at the expense of UDPhexose. The ratio [(14)C]UDPglucuronic acid/UDPhexose in cultures fed glucose or galactose was invariably low (0.15-0.2) regardless of the presence or absence of contact inhibition. 20 hr of hexose starvation invariably changed this ratio by a factor of 10 or more, due to accumulation of UDPglucuronic acid. This result was also observed in cultures transformed with polyoma virus. The presence of 3-O-methylglucose in the growth medium did not alter the typical "sugar starvation pattern" (i.e., the UDPglucuronic acid/UDPhexose ratio averaged 1.7). Enhancement of galactose uptake by hexose starvation was very pronounced in NIL cultures that were close to contact inhibition, but was not a prominent feature in the polyoma-transformed cultures. The transformed cells grown on glucose or galactose growth medium showed the usual enhanced rate of uptake of galactose as compared with nontransformed near-confluent cultures that had been fed hexose. The polyoma-induced enhancement showed none of the features characteristic of hexosestarved cells.
己糖摄取的增强似乎与肿瘤病毒诱导的细胞培养物转化以及接触抑制的缺失密切相关。己糖饥饿也会导致糖摄取增强。当监测仓鼠细胞培养物中(14)C标记的半乳糖在10或20分钟后的摄取情况时,这两种增强类型在仓鼠细胞培养物中都能得到清晰的证明。积累产物的图谱显著不同。在用多瘤病毒转化的仓鼠NIL细胞培养物中,大部分(14)C以UDP己糖的形式积累。未转化的细胞则积累半乳糖-1-磷酸以及UDP己糖。己糖饥饿的细胞显示出半乳糖摄取增强;然而,这种显著增强仅在接近接触抑制的NIL培养物中观察到。当用(14)C标记的半乳糖短暂孵育时,己糖饥饿细胞中出现的一个新的共同特征是以UDP己糖为代价,显著积累[(14)C]UDP葡萄糖醛酸。无论是否存在接触抑制,在以葡萄糖或半乳糖喂养的培养物中,[(14)C]UDP葡萄糖醛酸/UDP己糖的比值始终很低(0.15 - 0.2)。由于UDP葡萄糖醛酸的积累,20小时的己糖饥饿总是使这个比值变化10倍或更多。在用多瘤病毒转化的培养物中也观察到了这一结果。生长培养基中3 - O - 甲基葡萄糖的存在并未改变典型的“糖饥饿模式”(即UDP葡萄糖醛酸/UDP己糖比值平均为1.7)。己糖饥饿对半乳糖摄取的增强在接近接触抑制的NIL培养物中非常明显,但在多瘤病毒转化的培养物中并非显著特征。与用己糖喂养的未转化近汇合培养物相比,在葡萄糖或半乳糖生长培养基上生长的转化细胞显示出通常增强的半乳糖摄取速率。多瘤病毒诱导的增强没有表现出己糖饥饿细胞的任何特征。